FOXM1 Blocking Peptide
- Known as:
- FOXM1 Blocking Peptide
- Catalog number:
- BP301-532
- Product Quantity:
- 50 ug
- Category:
- Peptides
- Supplier:
- Beth
- Gene target:
- FOXM1 Blocking Peptide
Related genes to: FOXM1 Blocking Peptide
- Gene:
- FOXM1 NIH gene
- Name:
- forkhead box M1
- Previous symbol:
- FKHL16
- Synonyms:
- HFH-11, trident, HNF-3, INS-1, MPP2, MPHOSPH2, TGT3
- Chromosome:
- 12p13.33
- Locus Type:
- gene with protein product
- Date approved:
- 1997-07-25
- Date modifiied:
- 2016-10-05
Related products to: FOXM1 Blocking Peptide
Related articles to: FOXM1 Blocking Peptide
- Postoperative cognitive dysfunction (POCD) is a common post-anesthesia complication that seriously impairs patient prognosis. Microglial M1/M2 polarization imbalance is a key link in POCD development. Forkhead box M1 (FOXM1) is downregulated in sevoflurane (SEV)-induced cell models, but whether it affects microglial M1/M2 polarization remains unreported. qRT-PCR and Western blot were employed to detect the mRNA and protein levels. Flow cytometry was used to evaluate the expression of M1 markers and M2 markers in microglia. ELISA was employed to detect inflammatory factors. Cellular oxidative stress status and mitochondrial membrane potential (MMP) were assessed using commercial kits. GO functional annotation and KEGG pathway enrichment analyses were performed on the top 500 protein-coding genes downstream of FOXM1. Bioinformatic prediction, ChIP assay, and dual-luciferase reporter assay were used to verify the regulatory relationship between FOXM1 and regulator of G protein signaling 10 (RGS10). SEV treatment significantly decreased FOXM1 expression in HMC3 cells (P < 0.001, P < 0.01). FOXM1 overexpression alleviated SEV-induced M1/M2 polarization imbalance, reduced inflammation (lowered inflammatory factors), and mitigated oxidative stress (with reduced ROS/MDA, increased SOD/GSH-Px, and ameliorated MMP depolarization). GO/KEGG analysis revealed FOXM1 downstream genes were enriched in pathways like MAPK and TNF signaling pathways. FOXM1 bound to the RGS10 promoter and enhanced its transcription. RGS10 silencing reversed the ameliorative effects of FOXM1 overexpression on SEV-induced cellular changes (M1/M2 polarization, inflammation, oxidative stress, and MMP). FOXM1 regulates RGS10 via direct binding to its promoter, thereby modulating microglial M1/M2 polarization, inflammation, and oxidative stress. This study identifies the FOXM1-RGS10 axis as crucial for SEV-induced microglial dysfunction, providing experimental evidence for POCD mechanism elucidation and potential target screening. - Source: PubMed
Publication date: 2026/08/20
Zhang ChenLiu XiufengLiu Juan - Breast cancer is the most prevalent and lethal cancer among women worldwide. Although classification based on ERα, PR, and HER2 status guides treatment decisions, misclassification remains a challenge due to the complexity of ERα-associated transcriptional network. Identifying biomarkers that better reflect ERα activity may improve tumor stratification and therapeutic decision-making. We hypothesized that an ERα-related transcriptional framework could improve molecular characterization of breast cancer subtypes. - Source: PubMed
Publication date: 2026/08/05
Dozal-Luna Ana JazmínSantuario-Facio Sandra KCardona-Huerta ServandoGómez-Macías Gabriela SofíaRangel-Escareno ClaudiaLira-Albarrán SaúlGómez-Flores-Ramos LilianaOrtiz-López Rocío - Post-translational modifications (PTMs) critically regulate protein function, yet their intratumoral heterogeneity and clinical relevance in melanoma remain poorly characterized. Elucidating PTM-driven programs may uncover novel mechanisms of tumor progression and therapeutic vulnerability. - Source: PubMed
Publication date: 2026/08/13
Wu Man-NingZhou Dong-MeiZou Yue-MinYang Hao-YuBai Yan-Ping - Hyperactivation of the mineralocorticoid receptor (MR) causes pro-inflammatory and pro-fibrotic actions, which play a pivotal role in the pathophysiology of diabetic kidney disease (DKD). Finerenone (FIN), a novel non-steroidal mineralocorticoid receptor antagonist, attenuates glomerular endothelial cell fibrosis in diabetic mice, but the precise mechanism remains unclear. Therefore, This study investigates the mechanisms by which FIN improves glomerular endothelial cell fibrosis in diabetic mice. We used db/db mice to evaluate the effect of FIN on DKD in vivo. SEMA3C knockout mice and inhibition of SEMA3C in mesangial cells were used to evaluate the mechanism of FIN on glomerular fibrosis in vitro. Here we show that FIN treatment protected the kidneys against glomerular fibrosis in db/db mice. This effect was associated with mesangial cell-derived SEMA3C downregulation. Furthermore, knockout SEMA3C in vivo or knockdown of SEMA3C in vitro largely blocked the anti-fibrotic role of FIN. Moreover, we demonstrated that FIN inhibited SEMA3C expression mainly by inhibiting the KRAS/FOXM1 signaling pathway in glomerular mesangial cells of diabetic mice. Our findings elucidate a new molecular mechanism for the anti-fibrotic effect of FIN in DKD through inhibiting mesangial SEMA3C-mediated paracrine signaling, and highlight the pivotal role of FIN in preventing renal fibrosis by targeting SEMA3C. - Source: PubMed
Publication date: 2026/08/18
Wang YajingFeng YingjieLuo NaCao LingXu MengfanJi XinJu MengxianZong XicuiFang PenghuaZhang Zhenwen - Lysine β-hydroxybutyrylation (Kbhb) is a metabolite-derived post-translational modification of histone and non-histone proteins that couples β-hydroxybutyrate (BHB) availability to gene expression. Yet the transcription factors that govern the Kbhb substrate program in cancer remain unidentified. Existing studies have cataloged Kbhb-modified substrates or examined individual proteins, without identifying the transcriptional regulators of the program in a defined tumor context. Here, we performed network-based master regulator analysis (MRA), implemented in the viper package, on a molecular signature restricted to experimentally validated Kbhb substrates, across two independent PAM50 Basal-like breast cancer (BLBC) cohorts profiled on orthogonal platforms: TCGA-BRCA (RNA-seq; n = 195 tumor, 113 normal) and METABRIC (microarray; = 209 tumor, 148 normal). Dataset-specific regulatory networks were inferred with ARACNe-AP and integrated by cross-platform Stouffer meta-analysis. Of 1493 Kbhb substrates, 1322 and 1213 were expressed in the respective cohorts. The analysis identified seven concordant transcriptional master regulators (six activated, one repressed; cross-cohort NES correlation r = 0.64), with CENPA (meta-NES +4.55) and FOXM1 (meta-NES +4.27) as the dominant drivers. These findings nominate a BHB-Kbhb-FOXM1/CENPA axis linking ketone-body metabolism to mitotic transcription, with potentially protumoral implications for ketogenic regimens in BLBC. - Source: PubMed
Publication date: 2026/08/06
Tovar HugoHernández-Lemus Enrique